Search Result
Results for "
myocardial infarct size
" in MedChemExpress (MCE) Product Catalog:
1
Biochemical Assay Reagents
1
Isotope-Labeled Compounds
| Cat. No. |
Nombre del producto |
Target |
Áreas de investigación |
Chemical Structure |
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- HY-101415
-
|
Ubiquinone Q9; CoQ9; Ubiquinone 9
|
Apoptosis
Endogenous Metabolite
|
Cardiovascular Disease
|
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Coenzyme Q9 (Ubiquinone Q9), the major form of ubiquinone in rodents, is an amphipathic molecular component of the electron transport chain that functions as an endogenous antioxidant. Coenzyme Q9 attenuates the diabetes-induced decreases in antioxidant defense mechanisms. Coenzyme Q9 improves left ventricular performance and reduces myocardial infarct size and cardiomyocyte apoptosis .
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-
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- HY-17355A
-
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(R)-Pramipexole dihydrochloride; R-(+)-Pramipexole dihydrochloride; KNS-760704 dihydrochloride
|
ATP Synthase
Sodium Channel
Glutathione Peroxidase
NOD-like Receptor (NLR)
Mitophagy
Ferroptosis
PINK1/Parkin
Autophagy
Apoptosis
Reactive Oxygen Species (ROS)
|
Cardiovascular Disease
Neurological Disease
Inflammation/Immunology
|
|
Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more .
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- HY-103445
-
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Elastase
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Cardiovascular Disease
|
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SSR69071 is a potent, orally active and selective inhibitor of neutrophil elastase. SSR69071 reduces myocardial infarct size following ischemia-reperfusion injury . SSR69071 displays a higher affinity for human elastase (Ki=0.0168 nM) than for rat (Ki=3 nM), mouse (Ki=1.8 nM), and rabbit (Ki= 58 nM) elastases .
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- HY-N0430
-
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Coptisin
|
Indoleamine 2,3-Dioxygenase (IDO)
NF-κB
p38 MAPK
PI3K
Akt
Apoptosis
Reactive Oxygen Species (ROS)
Mitochondrial Metabolism
DNA/RNA Synthesis
ROCK
LDLR
|
Cardiovascular Disease
Neurological Disease
Metabolic Disease
Inflammation/Immunology
Cancer
|
|
Coptisine is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine can be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
|
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- HY-N0430A
-
|
|
Indoleamine 2,3-Dioxygenase (IDO)
NF-κB
p38 MAPK
PI3K
Akt
Apoptosis
Reactive Oxygen Species (ROS)
Mitochondrial Metabolism
DNA/RNA Synthesis
ROCK
LDLR
|
Cardiovascular Disease
Neurological Disease
Metabolic Disease
Inflammation/Immunology
Cancer
|
|
Coptisine Sulfate is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine Sulfate is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine Sulfate suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine Sulfate shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine Sulfate inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine Sulfate inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine Sulfate downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine Sulfate be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
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- HY-W011082
-
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NOD-like Receptor (NLR)
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Cardiovascular Disease
|
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NLRP3-IN-2, an intermediate substrate in the synthesis of glyburide, inhibits the formation of the NLRP3 inflammasome in cardiomyocytes and limits the infarct size following myocardial ischemia/reperfusion in the mouse, without affecting glucose metabolism .
|
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- HY-17355B
-
|
(R)-Pramipexole; R-(+)-Pramipexole; KNS-760704
|
PINK1/Parkin
Glutathione Peroxidase
Sodium Channel
ATP Synthase
NOD-like Receptor (NLR)
Mitophagy
Ferroptosis
Autophagy
Apoptosis
Reactive Oxygen Species (ROS)
|
Cardiovascular Disease
Neurological Disease
Inflammation/Immunology
|
|
Dexpramipexole ((R)-Pramipexole) is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more .
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- HY-164304
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-
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- HY-P1259A
-
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Proteasome
Bacterial
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Inflammation/Immunology
|
|
PR-39 TFA, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 TFAreversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 TFA stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice .
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- HY-128090A
-
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Aminopeptidase
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Cardiovascular Disease
|
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Apstatin TFA is a potent aminopeptidase P (APP) inhibitor with Ki values of 2.6, 0.64 µM for rat and human APP, respectively. Apstatin TFA shows cardioprotection .
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- HY-101415R
-
|
Ubiquinone Q9 (Standard); CoQ9 (Standard); Ubiquinone 9 (Standard)
|
Reference Standards
Apoptosis
Endogenous Metabolite
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Cardiovascular Disease
|
|
Coenzyme Q9 (Standard) is the analytical standard of Coenzyme Q9. This product is intended for research and analytical applications. Coenzyme Q9 (Ubiquinone Q9), the major form of ubiquinone in rodents, is an amphipathic molecular component of the electron transport chain that functions as an endogenous antioxidant. Coenzyme Q9 attenuates the diabetes-induced decreases in antioxidant defense mechanisms. Coenzyme Q9 improves left ventricular performance and reduces myocardial infarct size and cardiomyocyte apoptosis .
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- HY-106150
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EMD-96785
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Na+/H+ Exchanger (NHE)
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Others
|
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Eniporide (EMD 96785) is a Na(+)/H(+) exchange (NHE) inhibitor. Eniporide specifically inhibits the NHE-1 isoform. Eniporide improves cardiac performance inhibition associated with myocardial ischemia/reperfusion in animals, and limits infarct size in experimental models. Eniporide regulates cardiac performance and high-energy phosphate content in clinically relevant pig models of CPB and cardiac arrest .
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- HY-P1259
-
|
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Proteasome
Bacterial
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Inflammation/Immunology
|
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PR-39, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 reversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice .
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- HY-175640
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Pyroptosis
Reactive Oxygen Species (ROS)
Interleukin Related
Caspase
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Cardiovascular Disease
|
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Troponin-IN-1 is a troponin inhibitor. Troponin-IN-1 protects OGD/R-injured H9c2 cardiomyocytes by reducing LDH leakage, pyroptosis and ROS accumulation. Troponin-IN-1 inhibits NO production and IL-1β/TNF-α/IL-18 release in LPS (HY-D1056)-induced RAW264.7 cells. Troponin-IN-1 acts via caspase-1/GSDMD/IL-18 pathway. Troponin-IN-1 reduces myocardial infarct size in LAD-induced myocardial ischemia/reperfusion (MI/R) male rats. Troponin-IN-1 can be used for the study of myocardial ischemia/reperfusion (MI/R) injury .
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-
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- HY-17355BS
-
|
(R)-Pramipexole-d3 dihydrochloride; R-(+)-Pramipexole-d3 dihydrochloride; KNS-760704-d3 dihydrochloride
|
Isotope-Labeled Compounds
ATP Synthase
Sodium Channel
Glutathione Peroxidase
NOD-like Receptor (NLR)
Mitophagy
Ferroptosis
PINK1/Parkin
Autophagy
Apoptosis
Reactive Oxygen Species (ROS)
|
Cardiovascular Disease
Neurological Disease
Inflammation/Immunology
|
|
Dexpramipexole-d3 ((R)-Pramipexole-d3) dihydrochloride is the deuterium labeled Dexpramipexole. Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.
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-
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- HY-19230
-
|
|
Calmodulin
NO Synthase
CaMK
Calcineurin
Proteasome
Caspase
|
Cardiovascular Disease
|
|
DY-9760e is a calmodulin (CaM) inhibitor. DY-9760e selectively inhibits the activity of various calmodulin-dependent enzymes by antagonizing the Ca²⁺/CaM complex, exhibiting the strongest inhibitory activity against nNOS, CaM kinase II, and calcineurin (Ki: 0.9, 1.4, and 2.0 μM, respectively). DY-9760e inhibits excessive nitric oxide production and protein tyrosine nitration, as well as the activation of calpain and caspase-3. DY-9760e reduces infarct size, improves cardiac function, and inhibits oxidative stress and cell death. DY-9760e can be used in research on the treatment of myocardial infarction, cerebral ischemia, and other diseases .
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- HY-N2638
-
|
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Apoptosis
|
Cardiovascular Disease
|
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Ilexsaponin A, isolated from the root of Ilex pubescens, attenuates ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway. Ilexsaponin A can reduce myocardial infarct size, lower the serum levels of LDH, AST and CK-MB, increase cellular viability and inhibit apoptosis in hypoxia/reoxygenation cardiomyocytes .
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-
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- HY-P11124
-
|
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Apoptosis
PKC
Keap1-Nrf2
Heme Oxygenase (HO)
Drug Derivative
|
Neurological Disease
|
|
MGF24 is a modified protease-resistant MGF derivative. MGF24 protects dopaminergic neurons from 6-Hydroxydopamine (6-OHDA) (HY-113028)-induced apoptosis by inducing Heme oxygenase-1 (HO-1). MGF24 activates PKC-ε, which in turn activates Nrf2, up-regulating HO-1. MGF24 has neuroprotective activity and reduces myocardial infarct size in sheep models of myocardial ischemia. MGF24 can be used for neurological diseases like stroke, nerve injury and amyotrophic lateral sclerosis research .
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- HY-175675
-
|
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P2Y Receptor
Keap1-Nrf2
|
Cardiovascular Disease
Neurological Disease
|
|
P2Y1 antagonist 4 is a selective P2Y1 receptor antagonist with excellent blood-brain barrier (BBB) penetration.
P2Y1 antagonist 4 inhibits P2Y1 receptor-mediated cytosolic Ca 2+ increase (IC50 = 1.95 μM) and platelet aggregation (IC50 = 3.24 μM) induced by ADP in rabbit washed platelets. P2Y1 antagonist 4 significantly upregulates the level of nuclear Nrf2 protein in H2O2-treated HT22 cells. P2Y1 antagonist 4 reduces myocardial infarct size in a mouse acute myocardial infarction (MI) model. P2Y1 antagonist 4 can be used for the study of ischemic stroke and myocardial infarction .
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-
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- HY-128090
-
|
|
Aminopeptidase
|
Cardiovascular Disease
|
|
Apstatin is a potent aminopeptidase P (APP) inhibitor with Ki values of 2.6, 0.64 µM for rat and human APP, respectively. Apstatin shows cardioprotection .
|
-
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- HY-121726
-
|
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mTOR
Autophagy
|
Cardiovascular Disease
|
|
3HOI-BA-01 is amTORinhibitor.3HOI-BA-01reduces infarct size and inducedautophagyin a murine myocardial ischemia/reperfusion injury model .
|
-
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- HY-N2638R
-
|
|
Reference Standards
Apoptosis
|
Cardiovascular Disease
|
|
Ilexsaponin A (Standard) is the analytical standard of Ilexsaponin A. This product is intended for research and analytical applications. Ilexsaponin A, isolated from the root of Ilex pubescens, attenuates ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway. Ilexsaponin A can reduce myocardial infarct size, lower the serum levels of LDH, AST and CK-MB, increase cellular viability and inhibit apoptosis in hypoxia/reoxygenation cardiomyocytes .
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-
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- HY-19862
-
|
|
Na+/H+ Exchanger (NHE)
|
Cardiovascular Disease
|
|
TY-51924 ethanol sodium is a highly selective NHE-1 inhibitor (IC50 = 0.095 μM). TY-51924 ethanol sodium can significantly reduce the infarct size and myocardial enzyme release. TY-51924 ethanol sodium is commonly used in the study of ischemia-reperfusion injury .
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-
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- HY-106150A
-
|
|
Na+/H+ Exchanger (NHE)
|
Cardiovascular Disease
|
|
Eniporide mesylate (EMD 96785 mesylate) is a Na(+)/H(+) exchange (NHE) inhibitor. Eniporide mesylate specifically inhibits the NHE-1 isoform. Eniporide mesylate improves cardiac performance inhibition associated with myocardial ischemia/reperfusion in animals, and limits infarct size in experimental models. Eniporide mesylate regulates cardiac performance and high-energy phosphate content .
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-
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- HY-19129
-
|
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Prostaglandin Receptor
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Cardiovascular Disease
|
|
KT2-962 is a thromboxane A2 (TXA2) receptor antagonist and potent hydroxyl radical scavenger (IC50=500 nM). KT2-962 reduces myocardial infarct size and ventricular fibrillation. KT2-962 demonstrates cardioprotective effect in a canine ischemia/reperfusion model. KT2-962 is promising for research of myocardial ischemia-reperfusion injury and TXA2-mediated vascular diseases .
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-
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- HY-W011082R
-
|
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Reference Standards
NOD-like Receptor (NLR)
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Cardiovascular Disease
|
|
NLRP3-IN-2 (Standard) is the analytical standard of NLRP3-IN-2. This product is intended for research and analytical applications. NLRP3-IN-2, an intermediate substrate in the synthesis of glyburide, inhibits the formation of the NLRP3 inflammasome in cardiomyocytes and limits the infarct size following myocardial ischemia/reperfusion in the mouse, without affecting glucose metabolism .
|
-
-
- HY-121586
-
|
Bay g 6575
|
Lipoxygenase
|
Cardiovascular Disease
|
|
Nafazatrom (Bay g 6575) is an orally active cardioprotective agent that protects against ischemic damage. Nafazatrom dose-dependently inhibits neutrophil aggregation, superoxide anion generation, arachidonic acid metabolism, and to a lesser extent the release of β-glucosidase, platelet aggregation or arachidonic acid in vitro. Acid metabolism has no significant effect. In a dog ischemia-reperfusion model, Nafazatrom (10 mg/kg; po) reduced infarct size and the occurrence of arrhythmias and rescued ischemic myocardial function without affecting any hemodynamic changes. The basis of Nafazatrom's cardioprotection may be inhibition of neutrophil function and cellular infiltration in vitro .
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-
-
- HY-17355AR
-
|
(R)-Pramipexole dihydrochloride (Standard); R-(+)-Pramipexole dihydrochloride (Standard); KNS-760704 dihydrochloride (Standard)
|
Reference Standards
ATP Synthase
Sodium Channel
Glutathione Peroxidase
NOD-like Receptor (NLR)
Mitophagy
Ferroptosis
PINK1/Parkin
Autophagy
Apoptosis
|
Cardiovascular Disease
Neurological Disease
Inflammation/Immunology
|
|
Dexpramipexole ((R)-Pramipexole) dihydrochloride (Standard) is the analytical standard of Dexpramipexole (dihydrochloride). This product is intended for research and analytical applications. Dexpramipexole dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.
|
-
| Cat. No. |
Nombre del producto |
Type |
-
- HY-106150
-
|
EMD-96785
|
Biochemical Assay Reagents
|
|
Eniporide (EMD 96785) is a Na(+)/H(+) exchange (NHE) inhibitor. Eniporide specifically inhibits the NHE-1 isoform. Eniporide improves cardiac performance inhibition associated with myocardial ischemia/reperfusion in animals, and limits infarct size in experimental models. Eniporide regulates cardiac performance and high-energy phosphate content in clinically relevant pig models of CPB and cardiac arrest .
|
| Cat. No. |
Nombre del producto |
Target |
Research Area |
-
- HY-P1259A
-
|
|
Proteasome
Bacterial
|
Inflammation/Immunology
|
|
PR-39 TFA, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 TFAreversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 TFA stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice .
|
-
- HY-P1259
-
|
|
Proteasome
Bacterial
|
Inflammation/Immunology
|
|
PR-39, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 reversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice .
|
-
- HY-P11124
-
|
|
Apoptosis
PKC
Keap1-Nrf2
Heme Oxygenase (HO)
Drug Derivative
|
Neurological Disease
|
|
MGF24 is a modified protease-resistant MGF derivative. MGF24 protects dopaminergic neurons from 6-Hydroxydopamine (6-OHDA) (HY-113028)-induced apoptosis by inducing Heme oxygenase-1 (HO-1). MGF24 activates PKC-ε, which in turn activates Nrf2, up-regulating HO-1. MGF24 has neuroprotective activity and reduces myocardial infarct size in sheep models of myocardial ischemia. MGF24 can be used for neurological diseases like stroke, nerve injury and amyotrophic lateral sclerosis research .
|
| Cat. No. |
Nombre del producto |
Category |
Target |
Chemical Structure |
-
- HY-101415
-
-
-
- HY-N0430
-
|
Coptisin
|
Alkaloids
Structural Classification
Classification of Application Fields
Coptis chinensis Franch.
Ranunculaceae
Metabolic Disease
Quinoline Alkaloids
Plants
Disease Research Fields
Source Classification
|
Indoleamine 2,3-Dioxygenase (IDO)
NF-κB
p38 MAPK
PI3K
Akt
Apoptosis
Reactive Oxygen Species (ROS)
Mitochondrial Metabolism
DNA/RNA Synthesis
ROCK
LDLR
|
|
Coptisine is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine can be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
|
-
-
- HY-N0430A
-
|
|
Alkaloids
Structural Classification
Chelidonium majus
Classification of Application Fields
Metabolic Disease
Quinoline Alkaloids
Plants
Disease Research Fields
Papaveraceae
Source Classification
|
Indoleamine 2,3-Dioxygenase (IDO)
NF-κB
p38 MAPK
PI3K
Akt
Apoptosis
Reactive Oxygen Species (ROS)
Mitochondrial Metabolism
DNA/RNA Synthesis
ROCK
LDLR
|
|
Coptisine Sulfate is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine Sulfate is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine Sulfate suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine Sulfate shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine Sulfate inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine Sulfate inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine Sulfate downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine Sulfate be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
|
-
-
- HY-101415R
-
-
-
- HY-N2638
-
-
-
- HY-N2638R
-
-
| Cat. No. |
Nombre del producto |
Chemical Structure |
-
- HY-17355BS
-
|
|
|
Dexpramipexole-d3 ((R)-Pramipexole-d3) dihydrochloride is the deuterium labeled Dexpramipexole. Dexpramipexole ((R)-Pramipexole) dihydrochloride is an orally active, blood-brain barrier permeable mitochondrial protective agent. Dexpramipexole dihydrochloride upregulates the expression of Parkin, PINK1, GPX4 and FSP1; binds to mitochondrial F1/Fo-ATP synthase; blocks the Nav1.8 sodium channel; and inhibits the activation of the NLRP3 inflammasome. Dexpramipexole dihydrochloride induces mitophagy, inhibits ferroptosis, pyroptosis, apoptosis, neuroinflammation and eosinophilopoiesis; maintains mitochondrial function and redox homeostasis; reduces reactive oxygen species production; and decreases myocardial infarct size. Dexpramipexole dihydrochloride is applicable to studies on eosinophilic asthma, myocardial ischemia/reperfusion injury, sepsis-associated encephalopathy, analgesia, and more.
|
-
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